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The optimal exercise intensity and modality for maximizing cerebral blood flow (CBF) and hence potential exposure to positive, hemodynamically derived cerebral adaptations is yet to be fully determined. This study compared CBF velocity responses between running and cycling across a range of exercise intensities. Twenty‐six participants (12 females; age: 26 ± 8 years) completed four exercise sessions; two mode‐specific maximal oxygen consumption (VO2max) tests, followed by (order randomized) two incremental exercise protocols (3‐min stages at 35%, 50%, 65%, 80%, 95% VO2max). Continuous measures of middle cerebral artery velocity (MCAv), oxygen consumption, end‐tidal CO2 (PETCO2), and heart rate were obtained. Modality‐specific MCAv changes were observed for the whole group (interaction effect: p = .01). Exercise‐induced increases in MCAvmean during cycling followed an inverted‐U pattern, peaking at 65% VO2max (Δ12 ± 7 cm/s from rest), whereas MCAvmean during running increased linearly up to 95% VO2max (change from rest: Δ12 ± 13 vs. Δ7 ± 8 cm/s for running vs. cycling at 95% VO2max; p = .01). In contrast, both modalities had an inverted‐U pattern for PETCO2 changes, although peaked at different intensities (running: 50% VO2max, Δ6 ± 2 mmHg; cycling: 65% VO2max, Δ7 ± 2 mmHg; interaction effect: p = .01). Further subgroup analysis revealed that the running‐specific linear MCAvmean response was fitness dependent (Fitness*modality*intensity interaction effect: p = .04). Above 65% VO2max, fitter participants (n = 16; male > 45 mL/min/kg and female > 40 mL/min/kg) increased MCAvmean up to 95% VO2max, whereas in unfit participants (n = 7, male, This study compared cerebral blood flow (CBF) responses between running and cycling across a range of exercise intensities. Our findings demonstrate that exercise‐induced increases in CBF (as indexed from Doppler‐based measures of middle cerebral artery velocity, MCAv) during incremental running and cycling differ at higher exercise intensities, with the pattern of the MCAv response during running for fitter individuals dissociating from the regulatory influence of PCO2 at near maximal intensity (95% VO2max). Thus, modality‐specific differences in beat‐to‐beat flow patterns may alter CBF regulation processes and affect the complex integration of factors regulating CBF during exercise.

The effect that cardiorespiratory fitness has on the dynamic cerebral autoregulatory capacity during changes in mean arterial pressure (MAP) remains equivocal. Using a multiple-metrics approach, challenging MAP across the spectrum of physiological extremes (i.e. spontaneous through forced MAP oscillations), we characterized dynamic cerebral autoregulatory capacity in 19 male endurance athletes and 8 controls via three methods: [1] onset of regulation (i.e., time delay before an increase in middle cerebral artery (MCA) conductance [MCA flow velocity (MCAv)/mean arterial pressure (MAP)] and rate of regulation, after transient hypotension induced by sit-to-stand, and transfer function analysis (TFA) of MAP and MCAv responses during [2] spontaneous and [3] forced oscillations (5-min of squat-stand maneuvers performed at 0.05 and 0.10 Hz). Reductions in MAP and mean MCAv (MCAVmean) during initial orthostatic stress (0-30 s after sit-to-stand) and the prevalence of orthostatic hypotension were also determined. Onset of regulation was delayed after sit-to-stand in athletes (3.1±1.7 vs. 1.5±1.0 s; p=0.03), but rate of regulation was not different between groups (0.24±0.05 vs. 0.21±0.09 s-1; p=0.82). While both groups had comparable TFA metrics during spontaneous oscillations, athletes had higher TFA gain during 0.10 Hz squat-stand vs. recreational controls (p=0.01). Reductions in MAP (p=0.15) and MCAVmean (p=0.11) during orthostatic stress and the prevalence of initial orthostatic hypotension (p=0.65) were comparable between groups. These results indicate an intact ability of the cerebral vasculature to react to spontaneous oscillations but an attenuated capability to counter rapid and large changes in MAP in individuals with elevated cardiorespiratory fitness.New findingsWhat is the central question of this study?What is the impact of cardiorespiratory fitness on dynamic cerebral autoregulatory capacity?What is the main finding and its importance?Our results indicate an intact ability of the cerebral vasculature to react to spontaneous oscillations but an attenuated capability to counter rapid and large changes in mean arterial pressure in individuals with elevated cardiorespiratory fitness.

Hypercapnia impairs cerebrovascular control during rapid changes in blood pressure (BP); however, data concerning the effect of hypercapnia on steady state, nonpharmacological increases in BP is scarce. We recruited fifteen healthy volunteers (mean ± SD: age, 28 ± 6 years; body mass, 77 ± 12 kg) to assess the effect of hypercapnia on cerebrovascular control during steady‐state elevations in mean arterial BP (MAP), induced via lower body positive pressure (LBPP). Following 20 min of supine rest, participants completed 5 min of eucapnic 20 and 40 mm Hg LBPP (order randomized) followed by 5 min of hypercapnia (5% CO2 in air) with and without LBPP (order randomized), and each stage was separated by ≥5 min to allow for recovery. Middle cerebral artery blood velocity (MCAv), BP, partial pressure of end‐tidal carbon dioxide (PETCO2) and heart rate were recorded and presented as the change from the preceding baseline. No difference in MCAv was apparent between eupcapnic baseline and LBPPs (grouped mean 65 ± 11 cm·s−1, all P >0.05), despite the increased MAP with LBPP (Δ6 ± 5 and Δ8 ± 3 mm Hg for 20 and 40 mm Hg, respectively, both P 0.05), our findings indicate that hypercapnia impairs static autoregulation, such that higher blood pressures are translated into the cerebral circulation., This experiment investigated the effects of Hypercapnia on static cerebral autoregulation in healthy humans using lower body positive pressure mediated increases in MAP. It was found that nonpharmacological increases in MAP are translated to the cerebral circulation during hypercapnia.

The Valsalva maneuver (VM) produces large and abrupt increases in mean arterial pressure (MAP) at the onset of strain (Phase I), however, hypotension, sufficient to induce syncope, occurs upon VM release (phase III). We examined the effect of VM intensity and duration on middle cerebral artery blood velocity (MCAv) responses. Healthy men (n =10; mean ± SD: 26 ± 4 years) completed 30%, 60%, and 90% of their maximal VM mouth pressure, for 5 and 10 sec (order randomized) while standing. Beat‐to‐beat MCAv and MAP during phase I (peak), at nadir (phase III), and recovery are reported as the change from standing baseline. During phase I, MCAv rose 15 ± 6 cm·s−1 (P, More intense Valsalva maneuvers when standing are associated with an increase blood pressure response during Phase I of the maneuver although this is not accompanied by changes in cerebral blood flow. However, following the maneuver (phase III) more intense straining is associated with a greater decrease in both blood pressure and cerebral blood flow and in some instances is sufficient to induce syncope.